Eating broccoli retunes metabolism

31/07/2013 11:43:00

BBSRC-funded researchers at the Institute of Food Research have obtained the first evidence from human studies of how diets rich in glucosinolates, such as glucoraphanin found in broccoli, can 're-tune' cellular processes that get disrupted as we age.

Retuning these processes to normal may contribute to the reduced risk of cancer seen in people who eat diets rich in broccoli and similar vegetables. A high glucoraphanin broccoli variety, called Beneforté, is now available in UK supermarkets.

Inside each of our cells are specialised structures called mitochondria, which act as the engines of the cell. Mitochondria either burn up dietary fats and sugars to make energy or export them to be used by the cell as the building blocks to make other compounds needed for health. Mitochondria can also convert fats and sugars into forms for storage, which is how we can put on weight if we eat too much. For good health, we need to balance all these different metabolic activities.

Excessive fat or sugar in the diet can overload the mitochondrial machinery. Also, as we age, this machinery works less efficiently, especially if we do not have sufficient exercise. This is because of the build-up of Reactive Oxygen Species (ROS) in the mitochondria that inhibit some of the metabolic processes. The mitochondria may also begin to produce other compounds that can cause chronic inflammation. Disturbed metabolism and badly functioning mitochondria are associated with the development of chronic diseases such as obesity, Type II diabetes, cardiovascular disease and some forms of cancer.

To study what effects glucosinolate consumption has on metabolism, the researchers at the IFR carried out human dietary intervention trials. These involve making controlled and very specific changes to people's diets over a period of time, and provide the best possible evidence for the effects specific foods have on our bodies and metabolism.

48 volunteers were randomly split into three groups. Over a period of 12 weeks, one group ate high glucoraphanin broccoli, one group ate standard broccoli, and the third ate no broccoli. The researchers measured 346 metabolites in the blood before and after the 12 week period. They found that people who ate the high glucoraphanin broccoli had improved metabolism, and most of them had reduced levels of fatty acids in the blood and other lipid compounds that are associated with inflammation. They concluded that this was because of a bioactive compound called sulforaphane that is derived from glucoraphanin. This switched on 'antioxidant' genes which reduced the excessive ROS in the cells enabling their metabolic machinery to work better.

A number of studies have shown that diets rich in cruciferous vegetables may reduce the risk of cancer, type II diabetes and other chronic diseases of ageing through the actions of glucosinolates. This new study, published in the American Journal of Clinical Nutrition, provides the first evidence from human intervention trials of the mechanism behind this protective effect. This is being followed up by another study with a larger number of volunteers that is also looking at metabolism and biomarkers of cardiovascular health.

In 2011, a high glucoraphanin variety of broccoli was launched in UK supermarkets following significant investment in research from the Biotechnology and Biological Sciences Research Council (BBSRC). Beneforté 'super broccoli' represents a special achievement for UK bioscience: a consumer-focused, nutritionally-enhanced product. Beneforté broccoli was developed through traditional breeding techniques by the Institute of Food Research and the John Innes Centre on the Norwich Research Park, both of which receive strategic funding from BBSRC.

ENDS

Notes to editors

Reference: A diet rich in high glucoraphanin broccoli interacts with genotype to reduce discordance in plasma metabolite profiles through modulating mitochondrial disfunction, Charlotte N. Armah et al 10.3945/ajcn.113.065235 will be published by the American Journal of Clinical Nutrition on 31 July 2013.